Diet-induced adaptive thermogenesis requires neuropeptide FF receptor-2 signalling

Lei Zhang; Chi Kin Ip; I-Chieh J. Lee; Yue Qi; Felicia Reed; Tim Karl; Jac Kee Low; Ronaldo F. Enriquez; Nicola J. Lee; Paul A. Baldock; Herbert Herzog

doi:10.1038/s41467-018-06462-0

Diet-induced adaptive thermogenesis requires neuropeptide FF receptor-2 signalling

Lei Zhang, Chi Kin Ip, I-Chieh J. Lee, Yue Qi, Felicia Reed, Tim Karl, Jac Kee Low, Ronaldo F. Enriquez, Nicola J. Lee, Paul A. Baldock, Herbert Herzog

Western Sydney University

Research output: Contribution to journal › Article › peer-review

58 Citations (Scopus)

Abstract

Excess caloric intake results in increased fat accumulation and an increase in energy expenditure via diet-induced adaptive thermogenesis; however, the underlying mechanisms controlling these processes are unclear. Here we identify the neuropeptide FF receptor-2 (NPFFR2) as a critical regulator of diet-induced thermogenesis and bone homoeostasis. Npffr2âˆ’/âˆ’ mice exhibit a stronger bone phenotype and when fed a HFD display exacerbated obesity associated with a failure in activating brown adipose tissue (BAT) thermogenic response to energy excess, whereas the activation of cold-induced BAT thermogenesis is unaffected. NPFFR2 signalling is required to maintain basal arcuate nucleus NPY mRNA expression. Lack of NPFFR2 signalling leads to a decrease in BAT thermogenesis under HFD conditions with significantly lower UCP-1 and PGC-1Î± levels in the BAT. Together, these data demonstrate that NPFFR2 signalling promotes diet-induced thermogenesis via a novel hypothalamic NPY-dependent circuitry thereby coupling energy homoeostasis with energy partitioning to adipose and bone tissue.

Original language	English
Article number	4722
Number of pages	19
Journal	Nature Communications
Volume	9
DOIs	https://doi.org/10.1038/s41467-018-06462-0
Publication status	Published - 2018

Open Access - Access Right Statement

Â© The Author(s) 2018. This article is licensed under a Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/), which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder

Keywords

diet
homeostasis
mice as laboratory animals
neuropeptides
proteins

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1038/s41467-018-06462-0

Cite this

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title = "Diet-induced adaptive thermogenesis requires neuropeptide FF receptor-2 signalling",

abstract = "Excess caloric intake results in increased fat accumulation and an increase in energy expenditure via diet-induced adaptive thermogenesis; however, the underlying mechanisms controlling these processes are unclear. Here we identify the neuropeptide FF receptor-2 (NPFFR2) as a critical regulator of diet-induced thermogenesis and bone homoeostasis. Npffr2{\^a}ˆ{\textquoteright}/{\^a}ˆ{\textquoteright} mice exhibit a stronger bone phenotype and when fed a HFD display exacerbated obesity associated with a failure in activating brown adipose tissue (BAT) thermogenic response to energy excess, whereas the activation of cold-induced BAT thermogenesis is unaffected. NPFFR2 signalling is required to maintain basal arcuate nucleus NPY mRNA expression. Lack of NPFFR2 signalling leads to a decrease in BAT thermogenesis under HFD conditions with significantly lower UCP-1 and PGC-1{\^I}± levels in the BAT. Together, these data demonstrate that NPFFR2 signalling promotes diet-induced thermogenesis via a novel hypothalamic NPY-dependent circuitry thereby coupling energy homoeostasis with energy partitioning to adipose and bone tissue.",

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author = "Lei Zhang and Ip, {Chi Kin} and Lee, {I-Chieh J.} and Yue Qi and Felicia Reed and Tim Karl and Low, {Jac Kee} and Enriquez, {Ronaldo F.} and Lee, {Nicola J.} and Baldock, {Paul A.} and Herbert Herzog",

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AU - Zhang, Lei

AU - Ip, Chi Kin

AU - Lee, I-Chieh J.

AU - Qi, Yue

AU - Reed, Felicia

AU - Karl, Tim

AU - Low, Jac Kee

AU - Enriquez, Ronaldo F.

AU - Lee, Nicola J.

AU - Baldock, Paul A.

AU - Herzog, Herbert

PY - 2018

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N2 - Excess caloric intake results in increased fat accumulation and an increase in energy expenditure via diet-induced adaptive thermogenesis; however, the underlying mechanisms controlling these processes are unclear. Here we identify the neuropeptide FF receptor-2 (NPFFR2) as a critical regulator of diet-induced thermogenesis and bone homoeostasis. Npffr2âˆ’/âˆ’ mice exhibit a stronger bone phenotype and when fed a HFD display exacerbated obesity associated with a failure in activating brown adipose tissue (BAT) thermogenic response to energy excess, whereas the activation of cold-induced BAT thermogenesis is unaffected. NPFFR2 signalling is required to maintain basal arcuate nucleus NPY mRNA expression. Lack of NPFFR2 signalling leads to a decrease in BAT thermogenesis under HFD conditions with significantly lower UCP-1 and PGC-1Î± levels in the BAT. Together, these data demonstrate that NPFFR2 signalling promotes diet-induced thermogenesis via a novel hypothalamic NPY-dependent circuitry thereby coupling energy homoeostasis with energy partitioning to adipose and bone tissue.

AB - Excess caloric intake results in increased fat accumulation and an increase in energy expenditure via diet-induced adaptive thermogenesis; however, the underlying mechanisms controlling these processes are unclear. Here we identify the neuropeptide FF receptor-2 (NPFFR2) as a critical regulator of diet-induced thermogenesis and bone homoeostasis. Npffr2âˆ’/âˆ’ mice exhibit a stronger bone phenotype and when fed a HFD display exacerbated obesity associated with a failure in activating brown adipose tissue (BAT) thermogenic response to energy excess, whereas the activation of cold-induced BAT thermogenesis is unaffected. NPFFR2 signalling is required to maintain basal arcuate nucleus NPY mRNA expression. Lack of NPFFR2 signalling leads to a decrease in BAT thermogenesis under HFD conditions with significantly lower UCP-1 and PGC-1Î± levels in the BAT. Together, these data demonstrate that NPFFR2 signalling promotes diet-induced thermogenesis via a novel hypothalamic NPY-dependent circuitry thereby coupling energy homoeostasis with energy partitioning to adipose and bone tissue.

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KW - homeostasis

KW - mice as laboratory animals

KW - neuropeptides

KW - proteins

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M3 - Article

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JO - Nature Communications

JF - Nature Communications

M1 - 4722

ER -

Diet-induced adaptive thermogenesis requires neuropeptide FF receptor-2 signalling

Abstract

Open Access - Access Right Statement

Keywords

UN SDGs

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